CAJ | 학술논문

变应性接触性皮炎发病机制非常复杂,近来研究有新的发现,其中表皮角质形成细胞除促进T细胞的浸润外,还有限制该病发展的作用;皮肤树突细胞除执行抗原提呈作用外,可能还有免疫调节作用.还发现有新的免疫细胞和分子参与作用,如CD4+CD25+Foxp3+T细胞在其中发挥免疫抑制功能;Th17细胞介导、促进炎症反应;B10细胞通过IL-10依赖机制有负调节作用.一些黏附分子及其配基(PSGL-1等)和趋化因子(CCL21等)在发病中也起着一定作用.
변응성접촉성피염발병궤제비상복잡,근래연구유신적발현,기중표피각질형성세포제촉진T세포적침윤외,환유한제해병발전적작용;피부수돌세포제집행항원제정작용외,가능환유면역조절작용.환발현유신적면역세포화분자삼여작용,여CD4+CD25+Foxp3+T세포재기중발휘면역억제공능;Th17세포개도、촉진염증반응;B10세포통과IL-10의뢰궤제유부조절작용.일사점부분자급기배기(PSGL-1등)화추화인자(CCL21등)재발병중야기착일정작용.
The pathogenesis of allergic contact dermatitis (ACD) is very complicated. However, new discoveries have been made on the topic in recent studies. Epidermal keratinocytes not only promote T cell infiltration, but also limit the development of ACD. In addition, cutaneous dendritic cells possess both antigen presenting function and immunomodulatory activity. Furthermore, some immune cells and molecules have been newly demonstrated to be involved in the pathogenesis. For example, CD4+ CD25+ Foxp3+ T cells play a powerful immunosuppression role; T helper 17 (Th17) cells mediate and enhance inflammation reaction; B10 cells play a negative regulatory effect via an interleukin (IL)-10-dependent mechanism. Some adhesion molecules and their ligand (such as PSGL-1), as well as chemokines (such as CCL21) also exert a certain role in the pathogenesis of ACD.